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核内切核酸酶 G 控制卵巢癌细胞增殖。

Nuclear endonuclease G controls cell proliferation in ovarian cancer.

机构信息

Department of Biology, Kyung Hee University, Seoul, South Korea.

Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, Seoul, South Korea.

出版信息

FEBS Open Bio. 2023 Apr;13(4):655-669. doi: 10.1002/2211-5463.13572. Epub 2023 Feb 13.

DOI:10.1002/2211-5463.13572
PMID:36734593
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10068316/
Abstract

Ovarian cancer is characterized by a high degree of genetic heterogeneity. Platinum-based chemotherapy and some gene-targeted therapies have shown limited treatment efficacy due to toxicity and recurrence, and thus, it is essential to identify additional therapeutic targets based on an understanding of the pathological mechanism. Here, we report that endonuclease G, which exhibits altered expression in ovarian cancer, does not function as a cell death effector that digests chromosomal DNA in ovarian cancer. Endonuclease G is modulated by intracellular reactive oxygen species dynamics and plays a role in cell proliferation in ovarian cancer, suggesting that targeting endonuclease G alone or in combination with other antitumor agents may have the potential for development into a treatment for endonuclease G-overexpressing cancers, including ovarian cancer.

摘要

卵巢癌的特征是高度的遗传异质性。基于对病理机制的理解，铂类化疗和一些基因靶向治疗由于毒性和复发而显示出有限的治疗效果，因此，有必要根据其确定其他治疗靶点。在这里，我们报告在卵巢癌中表达改变的核酸内切酶 G 不作为一种细胞死亡效应物，不会在卵巢癌细胞中消化染色体 DNA。核酸内切酶 G 受到细胞内活性氧动力学的调节，在卵巢癌细胞增殖中发挥作用，这表明单独靶向核酸内切酶 G 或与其他抗肿瘤药物联合使用可能具有开发成治疗核酸内切酶 G 过表达癌症的潜力，包括卵巢癌。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/d923f70b3f58/FEB4-13-655-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/8e0eaeb8f002/FEB4-13-655-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/1aef2d42af78/FEB4-13-655-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/e83a33caaeba/FEB4-13-655-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/7518878a2790/FEB4-13-655-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/f6603ab20088/FEB4-13-655-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/419263447dff/FEB4-13-655-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/d923f70b3f58/FEB4-13-655-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/8e0eaeb8f002/FEB4-13-655-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/1aef2d42af78/FEB4-13-655-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/e83a33caaeba/FEB4-13-655-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/7518878a2790/FEB4-13-655-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/f6603ab20088/FEB4-13-655-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/419263447dff/FEB4-13-655-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c70/10068316/d923f70b3f58/FEB4-13-655-g007.jpg

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Cancer Drug Resist. 2022 May 12;5(2):424-435. doi: 10.20517/cdr.2022.13. eCollection 2022.
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